短期高脂肪饮食诱导肝脏ILC1分化与TLR9激活相关
Peng-Fei Hou1, Yu Yao1, Qian Bai1
1Research Center for Nutrition and Food Safety, Chongqing Key Laboratory of Nutrition and Health, Chongqing Medical Nutrition Research Center, Institute of Military Preventive Medicine, Third Military Medical University, Chongqing, PR China.
The Journal of nutritional biochemistry
|November 17, 2024
概括
短期高脂肪饮食显著增强肝脏2组先天性淋巴细胞 (ILC1s),增强免疫反应. 这通过托尔类受体9 (TLR9) 信号传递发生,提供了对饮食对肝脏免疫力影响的见解.
科学领域:
- 免疫学 免疫学 免疫学
- 营养科学 营养科学
- 肝病学 肝病学是一种肝病学.
背景情况:
- 食脂肪对免疫系统的影响,特别是肝脏免疫力,尚未完全理解.
- 肝脏2组先天性淋巴细胞 (ILC1s) 对于抗病毒防御,肝脏再生和伤害保护至关重要.
研究的目的:
- 为了研究短期高脂肪饮食对肝脏的影响 ILC1s.
- 阐明高脂肪饮食引起的肝脏变化的潜在机制 ILC1s.
主要方法:
- 鼠标模型接受了短期高脂肪饮食.
- 流细胞计测量量肝脏ILC1s. 的数量.
- EASY-RNAseq和ATAC-seq用于分析转录组和染色质可访问性.
- 用于探索机械路径的TLR9抑制剂.
主要成果:
- 2周高脂肪饮食增加了肝脏ILC1s的频率和数量.
- 在肝脏ILC1s中增加TNF-α的产生和TRAIL,CXCR3和CXCR6的表达.
- 转录组和染色质可访问性分析揭示了与淋巴细胞分化相关的途径.
- 高脂肪饮食引起的ILC1积累取决于TLR9信号传递.
结论:
- 短期高脂肪饮食通过TLR9介导机制促进肝脏ILC1的分化.
- 这些发现为调节肝脏区域免疫功能的营养策略提供了基础.
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